TY - JOUR
T1 - Exercise and diet-induced weight loss attenuates oxidative stress related-coronary vasoconstriction in obese adolescents
AU - Gao, Zhaohui
AU - Novick, Marsha
AU - Muller, Matthew
AU - Williams, Ronald
AU - Spilk, Samson
AU - Leuenberger, Urs
AU - Sinoway, Lawrence
N1 - Funding Information:
Acknowledgments We are thankful to Cheryl Blaha and Jessica Mast for their expert study coordination and invaluable technical assistance during the studies. The authors also express gratitude to Dr. Stephen E. Cyran and Jennie Stoner for consulting assistance and outstanding secretarial skills. Supported by R01 HL070222 (L.S.), M01 RR010732 (GCRC Grant), C06 RR016499 (Construction Grant) from the National Institutes of Health (L.S.) and in part, under a grant with the Pennsylvania Department of Health using Tobacco Settlement Funds (L.S.). The Department specifically disclaims responsibility for any analyses, interpretations or conclusions.
PY - 2013/2
Y1 - 2013/2
N2 - Obesity is a disease of oxidative stress (OS). Acute hyperoxia (breathing 100 % O2) can evoke coronary vasoconstriction by the oxidative quenching of nitric oxide (NO). To examine if weight loss would alter the hyperoxia-related coronary constriction seen in obese adolescents, we measured the coronary blood flow velocity (CBV) response to hyperoxia using transthoracic Doppler echocardiography before and after a 4-week diet and exercise regimen in 6 obese male adolescents (age 13-17 years, BMI 36.5 ± 2.3 kg/m 2). Six controls of similar age and BMI were also studied. The intervention group lost 9 ± 1 % body weight, which was associated with a reduced resting heart rate (HR), reduced diastolic blood pressure (BP), and reduced RPP (all P < 0.05). Before weight loss, hyperoxia reduced CBV by 33 ± 3 %. After weight loss, CBV only fell by 15 ± 3 % (P < 0.05). In the control group, CBV responses to hyperoxia were unchanged during the two trials. Thus weight loss: (1) reduces HR, BP, and RPP; and (2) attenuates the OS-related coronary constrictor response seen in obese adolescents. We postulate that: (1) the high RPP before weight loss led to higher myocardial O 2 consumption, higher coronary flow and greater NO production, and in turn a large constrictor response to hyperoxia; and (2) weight loss decreased myocardial oxygen demand and NO levels. Under these circumstances, hyperoxia-induced vasoconstriction was attenuated.
AB - Obesity is a disease of oxidative stress (OS). Acute hyperoxia (breathing 100 % O2) can evoke coronary vasoconstriction by the oxidative quenching of nitric oxide (NO). To examine if weight loss would alter the hyperoxia-related coronary constriction seen in obese adolescents, we measured the coronary blood flow velocity (CBV) response to hyperoxia using transthoracic Doppler echocardiography before and after a 4-week diet and exercise regimen in 6 obese male adolescents (age 13-17 years, BMI 36.5 ± 2.3 kg/m 2). Six controls of similar age and BMI were also studied. The intervention group lost 9 ± 1 % body weight, which was associated with a reduced resting heart rate (HR), reduced diastolic blood pressure (BP), and reduced RPP (all P < 0.05). Before weight loss, hyperoxia reduced CBV by 33 ± 3 %. After weight loss, CBV only fell by 15 ± 3 % (P < 0.05). In the control group, CBV responses to hyperoxia were unchanged during the two trials. Thus weight loss: (1) reduces HR, BP, and RPP; and (2) attenuates the OS-related coronary constrictor response seen in obese adolescents. We postulate that: (1) the high RPP before weight loss led to higher myocardial O 2 consumption, higher coronary flow and greater NO production, and in turn a large constrictor response to hyperoxia; and (2) weight loss decreased myocardial oxygen demand and NO levels. Under these circumstances, hyperoxia-induced vasoconstriction was attenuated.
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U2 - 10.1007/s00421-012-2459-9
DO - 10.1007/s00421-012-2459-9
M3 - Article
C2 - 22814577
AN - SCOPUS:84872292303
SN - 1439-6319
VL - 113
SP - 519
EP - 528
JO - European Journal of Applied Physiology
JF - European Journal of Applied Physiology
IS - 2
ER -
